An Experimental Study Of Nitric Oxide Mechanism On Dingxin Recipe And Tanshinone â…¡ A In Preventing Arrhythmia

Objective: To observe the influence of nitric oxide(NO) on experimental arrhythmic rats, investigate the mechanism of Dingxin Recipe(DXR) and tanshinone II A (Tan) in preventing and treating arrhythmia. Methods: Arrhythmia models were made by aconitine intravenous injection from venae femoralis and coronary artery ligation respectively. NO level in the serum was measured by NO reagent kits and relationship between arrhythmia and NO level was analysed at the same time. The influence of L- Arginine(Arg), DXR and Tan on NO level in the blood was measured. Flow cytometry was used to detect the expression of whole blood platelet membrane adhesion molecules to observe the effects of DXR and Tan on arrhythmia and platelet membrane adhesion molecules. Intracellular calcium concentration[Ca2~]1, cell membrane potential(MP) and n-titochondria membrane potential(MMP) in the cultured myocytes were determined with adherent cell analysis and sorting system. Serum that contain DXR was prepared by serulogic pharmacological method. The effects of DXR and Tan on [Ca2~], MP and MMP was observed. Results: 1. Arg increased the NO level in the serum and reduced the occurrence of arrhythmia. DXR and 憆an decreased the happen of arrhythmia by increasing NO level in the blood. There was significant difference comparing with placebo control group and the effect was related to the concentration. L-N-Nitro-Arginine Methyl Ester(L-NAME) could inhibit the action of Arg and Tan, but couldn抰 suppress the action of DXR. 2. DXR, Tan and Arg reduced arrhythmia by decreasing the expression of CD4 I and CD62P(P-selectin) which were the markers of platelet activation. L-NAME can inhibit Arg and Tan抯 anti-arrhythmic and anti-platelet aggregation effects, but not DXR抯. 3. Hypoxia raised [Ca21~ but lowered the level of MP and MMP in cardiac myocytes. The serum of DXR lowered [Ca2~]~ in the normal and hypoxia cardiac myocytes, ameliorate the fall of MP and MMP induced by hypoxia and maintain MP and MMP level near the baseline. L ?? NAME can inhibit the action of Arg and Tan but not of DXR. Conclusions: 1. The relationship between NO and the occurrence of arrhythmia was negative correlation. 2. DXR could increase the NO level, decrease the expression of CD41 and CD62P and regulate the level of [Ca2+]i, MP and MMP. Then the happen of experimental arrhythmia was reduced. L-NAME couldn抰 inhibit the action of DXR. 3. Tan increased the level of NO, decreased the expression of platelet membrane adhesion molecules and regulated the level of [Ca2+]i, MP and MMP to decrease the happening of arrhythmia. L-NAME could inhibit the action of Tan.